Dendritic Na inactivation drives a decrease in ISI (Fernandez et al 2005)

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Accession:59480
We use a combination of dynamical analysis and electrophysiological recordings to demonstrate that spike broadening in dendrites is primarily caused by a cumulative inactivation of dendritic Na(+) current. We further show that a reduction in dendritic Na(+) current increases excitability by decreasing the interspike interval (ISI) and promoting burst firing.
Reference:
1 . Fernandez FR, Mehaffey WH, Turner RW (2005) Dendritic na+ current inactivation can increase cell excitability by delaying a somatic depolarizing afterpotential. J Neurophysiol 94:3836-48 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): ELL pyramidal cell;
Channel(s): I Na,t; I K;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: MATLAB;
Model Concept(s): Activity Patterns; Dendritic Action Potentials; Active Dendrites;
Implementer(s): Fernandez FR [ffernand at ucalgary.ca]; Mehaffey WH ;
Search NeuronDB for information about:  I Na,t; I K;
  
/
na_excit
readme.txt
ELLburstpyramidal.m
ELLburstpyramidal_noSigProcToolbox.m
fig2b.jpg
                            
This is the readme for the model associated with the paper:

Fernandez FR, Mehaffey WH, Turner RW (2005) Dendritic na+ current
inactivation can increase cell excitability by delaying a somatic
depolarizing afterpotential. J Neurophysiol 94:3836-48

Hotchkiss Brain Institute, University of Calgary, 3330 Hospital
Dr. N.W., Calgary, Alberta T2N 4N1, Canada.
rwturner@ucalgary.ca.

Many central neurons support active dendritic spike
backpropagation mediated by voltage-gated currents. Active spikes
in dendrites have been shown capable of providing feedback to the
soma to influence somatic excitability and firing dynamics
through a depolarizing afterpotential (DAP). In pyramidal cells
of the electrosensory lobe of weakly electric fish, Na(+) spikes
in dendrites undergo a frequency-dependent broadening that
enhances the DAP to increase somatic firing frequency. We use a
combination of dynamical analysis and electrophysiological
recordings to demonstrate that spike broadening in dendrites is
primarily caused by a cumulative inactivation of dendritic Na(+)
current. We further show that a reduction in dendritic Na(+)
current increases excitability by decreasing the interspike
interval and promoting burst firing. This process arises when
inactivation of dendritic Na(+) current shifts the latency of the
dendritic spike to delay the arrival of the DAP sufficiently to
increase its impact on somatic membrane potential despite a
reduction in dendritic excitability. Furthermore, the
relationship between dendritic Na(+) current density and somatic
excitability is nonmonotonic, as intermediate levels of dendritic
Na(+) current exert the greatest excitatory influence. These
results reveal that temporal shifts in dendritic spike firing
provide a novel means for backpropagating spikes to influence the
final output of a cell.

These files were supplied by Dr Fernandez
ffernand@ucalgary.ca

If you have the sigmal processing toolbox you can run the matlab 
program ELLburstpyramidal.m, otherwise run the matlab program 
ELLburstpyramidal_noSigProcToolbox.m

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